热休克对缺氧复氧损伤的心肌细胞产生一氧化氮的影响  

The influence of hypoxia /reoxygenation on production and release of nitric oxide from cultured new- born rat cardiomyocytes

作　　者：魏刘华[1] 朱洪生[1] 

机构地区：[1]上海第二医科大学附属仁济医院心胸外科,200001

出　　处：《中华医学杂志》1996年第9期697-699,共3页National Medical Journal of China

基　　金：国家自然科学基金资助项目

摘　　要：目的 探讨热休克预处理对心肌细胞保护作用的机理。方法作者在培养的新生大鼠心肌细胞的模型上，观察缺氧、复氧对培养心肌细胞产生和释放一氧化氮（ＮＯ）、乳酸脱氢酶（ＬＤＨ）和磷酸肌酸激酶（ＣＰＫ）的影响。实验共分为４组：１．对照组；２．损伤组（加无糖无氧Ｈａｎｋ＇ｓ液，充入氮气以置换瓶内空气）；３．热休克处理组（细胞培养瓶放入４２℃水浴箱中孵育１小时）；４．地塞米松组（在无氧Ｈａｎｋ＇ｓ液中加入地塞米松）。结果培养心肌细胞缺氧３小时、复氧３０分钟后ＮＯ的产生显著增加，ＣＰＫ、ＬＤＨ的释放也显著升高。热休克（细胞在４２℃水浴１小时，恢复２４小时）或地塞米松（１０ｍｏｌ／Ｌ）预处理可显著减少心肌细胞ＮＯ、ＬＤＨ和ＣＰＫ的产生和释放。结论提示心肌细胞在缺氧、复氧过程中产生的大量ＮＯ对培养心肌细胞是有毒的。热休克预处理对缺氧、复氧损伤的培养心肌细胞的保护作用与抑制过量ＮＯ的产生有关。Objectlve To study the influence of hypoxia/reoxygenation on the production and release of nitric oxide (NO) , lactate dehydrogenase CLDH) and creatine kinase (CPK ) from cultured newborn rat car- diomyocytes. Methods The rats were divided into four groups : control , hypoxia/reoxy-genation , heat shock pretreated , dexamethasone pretreated. Results After 3 hours of hypoxia and 30 minutes of re- oxygenation , the content of NO in the supernatent of cardiomyocytes increased significantly ( P < 0. 05) , which was accompanied by an increase in the release of LDH and CPK (P<0. 001 , P<0. 001 respectively ). When pretreated by the heat shock (expcaed to 42 ℃ for 1 hour and then allowed to re- cover for 24 hours) or by applying dexamethasone at the onset of hypoxia , the production and release of NO , LDH , CPK decreased markedly (P< 0. 05 ) . Conclusions Exceasive release of NO may play an important role in the reperfusion injury of cardiomyocytes. Heat shock seems to provide protection for cardiomyacytes from hypoxia /reoxygenation injury. The mechanism may be related to the inhibition of excessive release of No from the cardiomyocytes,

关 键 词：缺氧症 复氧 心肌细胞 热休克 心肌缺氧 

分 类 号：R364.4[医药卫生—病理学]